Fig 1: Sodium palmitate represses the viability of LO2 cells. (A) CCK-8 assay was performed to determine the effects of various concentrations of sodium palmitate (25, 50, 75, 100, 125 and 150 µmol/l) on LO2 human liver cells treated for 12, 24 and 48 h. ^P<0.05 and ^^P<0.01 vs. Control. (B) CCK-8 assay was used to measure the effect of LSDP5 on cell viability in LO2 cells treated with 100 µmol/l sodium palmitate for 48 h (Model). *P<0.05 vs. Control; ^P<0.05 vs. Model. LSDP5, lipid storage droplet protein 5; M, model; NC, negative control.
Fig 2: LSDP5 expression in LO2 cells. (A and B) Experiments were divided into Control group (0.1% PBS treatment), Model group (100 µmol/l sodium palmitate treatment), NC group (Model cells transfected with pCMV5-NC plasmid) and LSDP5 group (Model cells transfected with pCMV5-LSDP5 overexpression plasmid), and the (A) mRNA and (B) protein expression levels were determined reverse transcription-quantitative polymerase chain reaction and western blotting, respectively; ß-actin served as an internal control and for normalization. ^P<0.05 vs. Model. LSDP5, lipid storage droplet protein 5; M, model; NC, negative control.
Fig 3: LSDP5 reduces apoptosis in LO2 lipotoxicity Model cells. (A) Apoptosis was detected by Annexin V-FITC/PI apoptosis detection kit. (B) mRNA expression levels of Bax and Bcl-2 were measured by reverse transcription-quantitative polymerase chain reaction. (C and D) Protein expression levels of active-caspase-3, Bax and Bcl-2 were measured by western blot assay; ß-actin was used as a loading control and for normalization. *P<0.05, **P<0.01 and ***P<0.001 vs. Control; ^P<0.05 and ^^P<0.01 vs. Model. Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma-2; FITC, fluorescein isothiocyanate; LSDP5, lipid storage droplet protein 5; M, model; NC, negative control; PI, propidium iodide.
Fig 4: LSDP5 reduces mitochondrial damage in LO2 lipotoxicity Model. (A) MMP rates were detected by JC-1 kit. (B) mRNA expression levels of Cytc, Cox IV and CPT1a were measured by reverse transcription-quantitative polymerase chain reaction. (C and D) Protein expression levels of Cytc, Cox IV and CPT1a were measured by western blot assay; ß-actin was used as a loading control and for normalization. *P<0.05 and **P<0.01 vs. Control; ^P<0.05 vs. Model. Cox IV, cytochrome c oxidase subunit IV; CPT1a, carnitine palmitoyltransferase 1a; Cytc, cytochrome c; LSDP5, lipid storage droplet protein 5; M, model; MMP, mitochondrial membrane potential; NC, negative control.
Fig 5: LSDP5 regulates lipid metabolism-related factors in LO2 lipotoxicity Model cells. (A and B) ACC1, ACC2, Fas and PPARa (A) mRNA and (B) protein expression levels were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively; ß-actin served as an internal control and for normalization. *P<0.05 and **P<0.01 vs. Control; ^P<0.05 and ^^P<0.01 vs. Model. ACC, acetyl-co A carboxylase1; Fas, fatty acid synthase; LSDP5, lipid storage droplet protein 5; M, model; NC, negative control.
Supplier Page from Abcam for Anti-LSDP5 antibody